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The vitamin D receptor (VDR) is a nuclear transcriptional regulator that activates by binding to 1a,25-dihydroxycholecalciferol (1a,25(OH)2D), known as calcitriol, which forms a heterodimer with the retinoid X receptor (RXR). Calcitriol signalling is involved various biological processes that include the metabolic processes of calcium and phosphorous as well as parathormone release, cellular growth and regulation of adaptive and innate immunity.
A T >C change in the promoter region of the VDR variant (rs11568820) eliminates the binding site of the transcription factor Cdx2 just upstream of exon 1. This leads to a smaller protein with reduced transcriptional activity. The F variant is found in high frequency among Asians and Europeans, and in low frequency among Sub-Saharan Africans.
The findings of this study enhance our understanding of the role that VDR gene polymorphisms can have in regulating the response to supplementation with calcitriol. Carriers of the TaqI polymorphism and the FF genotype of the FokI polymorphism have higher transcriptional activation of VDR and are associated with increased calcium absorption and bone mineral density, as well as reduced risk of fractures [34, 35]. Further research with an unbiased design is required to improve our understanding of how these genetic variants affect vitamin D supplementation and its clinical significance.